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Introduction: The aim of this research was to clarify the mechanism through which baicalin exerts its inhibitory effects on Aeromonas hydrophila infection. Methods: The antibacterial efficacy of baicalin was assessed by determining its minimum inhibitory concentration (MIC) against A. hydrophila. Various parameters, including the growth curve, cell wall integrity, biofilm formation, AKP content, and morphological alterations of A. hydrophila, were analyzed. In vivo experiments involved the administration of A. hydrophila 4 h postintraperitoneal injection of varying doses of baicalin to induce infection, with subsequent monitoring of mortality rates. After a 3 d period, liver, spleen, and intestinal tissues were harvested to evaluate organ indices, antioxidant and immune parameters, as well as intestinal microbial composition. Results: The findings indicated that baicalin treatment resulted in the disruption of the cell wall of A. hydrophila, leading to the loss of its normal structural integrity. Furthermore, baicalin significantly inhibited biofilm formation and facilitated the release of intracellular proteins (P < 0.05). In vivo, baicalin enhanced the survival rates of yellow catfish infected with A. hydrophila. Compared to the control group, the liver index of yellow catfish was elevated, while the spleen and intestinal indices were reduced in the baicalin-treated group (P < 0.05). Additionally, baicalin at an appropriate dosage was found to increase levels of SOD, GSH, CAT, ACP, and AKP in yellow catfish (P < 0.05), while simultaneously decreasing MDA accumulation and the mRNA expression of inflammatory markers such as Keap1, IL1, IFN-g, and TNF-a, (P < 0.05). Moreover, baicalin significantly enhanced the operational taxonomic unit (OTU) count in A. hydrophila-infected yellow catfish (P < 0.05), restoring the abundance of Barnesiellaceae, Enterobacteriaceae, Plesiomonas, and UBA1819 (P < 0.05). Discussion: In summary, baicalin demonstrates the potential to improve the survival rate of yellow catfish subjected to A. hydrophila infection, augment antioxidant and immune responses, mitigate inflammation, and enhance intestinal microbial diversity. [ABSTRACT FROM AUTHOR]

BACKGROUND: Growing evidence indicates that trimethylamine N-oxide, a gut microbial metabolite of dietary choline and carnitine, promotes both cardiovascular disease and chronic kidney disease risk. It remains unclear how circulating concentrations of trimethylamine N-oxide and its related dietary and gut microbe-derived metabolites (choline, betaine, carnitine, γ-butyrobetaine, and crotonobetaine) affect incident heart failure (HF). METHODS: We evaluated 11 768 participants from the Cardiovascular Health Study and the Multi-Ethnic Study of Atherosclerosis with serial measures of metabolites. Cox proportional hazard models were used to examine the associations between metabolites and incident HF, adjusted for cardiovascular disease risk factors. RESULTS: In all, 2102 cases of HF occurred over a median follow-up of 15.9 years. After adjusting for traditional risk factors, higher concentrations of trimethylamine N-oxide (hazard ratio, 1.15 [95% CI, 1.09-1.20]; P<0.001), choline (hazard ratio, 1.44 [95% CI, 1.26-1.64]; P<0.001), and crotonobetaine (hazard ratio, 1.24 [95% CI, 1.16-1.32]; P<0.001) were associated with increased risk for incident HF. After further adjustment for renal function (potential confounder or mediator), these associations did not reach Bonferroni-corrected statistical significance (P=0.01, 0.049, and 0.006, respectively). Betaine and carnitine were nominally associated with a higher incidence of HF (P<0.05). In exploratory analyses, results were similar for subtypes of HF based on left ventricular ejection fraction, and associations appeared generally stronger among Black and Hispanic/Latino versus White adults, although there were no interactions for any metabolites with race. CONCLUSIONS: In this pooled analysis of 2 well-phenotyped, diverse, community-based cohorts, circulating concentrations of gut microbe-derived metabolites such as trimethylamine N-oxide, choline, and crotonobetaine were independently associated with a higher risk of developing HF. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and cognitive impairment. It severely affects the quality of life of victims. The prevalence of AD has been increasing in recent years. Therefore, it is of great importance to elucidate the pathogenic mechanism of AD and search for effective therapeutic approaches. Gut microbiota dysbiosis, an altered state of gut microbiota, has been well known for its involvement in the pathogenesis of AD. Much effort has been made in searching for approaches capable of modulating the composition of gut microbiota in recent years. Herbal medicines have attracted extensive attention in recent decades for the prevention and treatment of AD. Here, we gave an overview of the recent research progress on the modulatory effects of herbal medicines and herbal formulae on gut microbiota as well as the possible beneficial effects on AD, which may provide new insights into the discovery of anti-AD agents and their therapeutic potential for AD through modulating the composition of gut microbiota. [ABSTRACT FROM AUTHOR]

A high-fat diet (HFD) is a high-risk factor for the malignant progression of cancers through the disruption of the intestinal microbiota. However, the role of the HFD-related gut microbiota in cancer development remains unclear. This study found that obesity and obesity-related gut microbiota were associated with poor prognosis and advanced clinicopathological status in female patients with breast cancer. To investigate the impact of HFD-associated gut microbiota on cancer progression, we established various models, including HFD feeding, fecal microbiota transplantation, antibiotic feeding, and bacterial gavage, in tumor-bearing mice. HFD-related microbiota promotes cancer progression by generating polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Mechanistically, the HFD microbiota released abundant leucine, which activated the mTORC1 signaling pathway in myeloid progenitors for PMN-MDSC differentiation. Clinically, the elevated leucine level in the peripheral blood induced by the HFD microbiota was correlated with abundant tumoral PMN-MDSC infiltration and poor clinical outcomes in female patients with breast cancer. These findings revealed that the "gut--bone marrow--tumor" axis is involved in HFD-mediated cancer progression and opens a broad avenue for anticancer therapeutic strategies by targeting the aberrant metabolism of the gut microbiota. [ABSTRACT FROM AUTHOR]

Background: The dysbiosis of gut microbiota (GM) is considered a contributing factor to prostatitis, yet the causality remains incompletely understood. Methods: The genome-wide association study (GWAS) data for GM and prostatitis were sourced from MiBioGen and FinnGen R10, respectively. In the two-sample Mendelian randomization (MR) analysis, inverse variance weighting (IVW), MR-Egger, weighted median, simple mode, weighted mode, and maximum likelihood (ML) methods were utilized to investigate the causal relationship between GM and prostatitis. A series of sensitivity analysis were conducted to confirm the robustness of the main results obtained from the MR analysis. Results: According to the IVW results, genus Sutterella (OR: 1.37, 95% CI: 1.09--1.71, p = 0.006) and genus Holdemania (OR: 1.21, 95% CI: 1.02-- 1.43, p = 0.028) were associated with an increased risk of prostatitis. The phylum Verrucomicrobia (OR: 0.76, 95% CI: 0.58--0.98, p = 0.033) and genus Parasutterella (OR: 0.84, 95% CI: 0.70--1.00, p = 0.045) exhibited a negative association with prostatitis, indicating a potential protective effect. Sensitivity analysis showed that these results were not affected by heterogeneity and horizontal pleiotropy. Furthermore, the majority of statistical methods yielded results consistent with those of the IVW analysis. Conclusions: In this study, we identified two GM taxon that might be protective against prostatitis and two GM taxon that could increase the risk of developing prostatitis. These findings could potentially provide a valuable theoretical basis for the future development of preventive and therapeutic strategies for prostatitis. [ABSTRACT FROM AUTHOR]

Background: An increasing body of evidence suggests a profound interrelation between the microbiome and sleep-related concerns. Nevertheless, current observational studies can merely establish their correlation, leaving causality unexplored. Study objectives: To ascertain whether specific gut microbiota are causally linked to seven sleep-related characteristics and propose potential strategies for insomnia prevention. Methods: The study employed an extensive dataset of gut microbiota genetic variations from the MiBioGen alliance, encompassing 18,340 individuals. Taxonomic classification was conducted, identifying 131 genera and 196 bacterial taxa for analysis. Sleep-related phenotype (SRP) data were sourced from the IEU OpenGWAS project, covering traits such as insomnia, chronotype, and snoring. Instrumental variables (IVs) were selected based on specific criteria, including locus-wide significance, linkage disequilibrium calculations, and allele frequency thresholds. Statistical methods were employed to explore causal relationships, including inverse variance weighted (IVW), MR-Egger, weighted median, and weighted Mode. Sensitivity analyses, pleiotropy assessments, and Bonferroni corrections ensured result validity. Reverse causality analysis and adherence to STROBE-MR guidelines were conducted to bolster the study's rigor. Results: Bidirectional Mendelian randomization (MR) analysis reveals a causative interplay between selected gut microbiota and sleep-related phenotypes. Notably, outcomes from the rigorously Bonferroni-corrected examination illuminate profound correlations amid precise compositions of the intestinal microbiome and slumber-associated parameters. Elevated abundance within the taxonomic ranks of class Negativicutes and order Selenomonadales was markedly associated with heightened susceptibility to severe insomnia (OR = 1.03, 95% CI: 1.02-1.05, p = 0.0001). Conversely, the augmented representation of the phylum Lentisphaerae stands in concord with protracted sleep duration (OR = 1.02, 95% CI: 1.01-1.04, p = 0.0005). Furthermore, heightened exposure to the genus Senegalimassilia exhibits the potential to ameliorate the manifestation of snoring symptoms (OR = 0.98, 95% CI: 0.96-0.99, p = 0.0001). Conclusion: This study has unveiled the causal relationship between gut microbiota and SRPs, bestowing significant latent value upon future endeavors in both foundational research and clinical therapy.1.04, p = 0.0005). Furthermore, heightened exposure to the genus Senegalimassilia exhibits the potential to ameliorate the manifestation of snoring symptoms (OR = 0.98, 95% CI: 0.96-0.99, p = 0.0001). [ABSTRACT FROM AUTHOR]

Introduction: Numerous studies have suggested an association between gut microbiota and polycystic ovarian syndrome (PCOS). However, the causal relationship between these two factors remains unclear. Methods: A review of observational studies was conducted to compare changes in gut microbiota between PCOS patients and controls. The analysis focused on four levels of classification, namely, phylum, family, genus, and species/genus subgroups. To further investigate the causal relationship, Mendelian randomization (MR) was employed using genomewide association study (GWAS) data on gut microbiota from the MiBioGen consortium, as well as GWAS data from a large meta-analysis of PCOS. Additionally, a reverse MR was performed, and the results were verified through sensitivity analyses. Results: The present review included 18 observational studies that met the inclusion and exclusion criteria. The abundance of 64 gut microbiota taxa significantly differed between PCOS patients and controls. Using the MR method, eight bacteria were identified as causally associated with PCOS. The protective effects of the genus Sellimonas on PCOS remained significant after applying Bonferroni correction. No significant heterogeneity or horizontal pleiotropy was found in the instrumental variables (IVs). Reverse MR analyses did not reveal a significant causal effect of PCOS on gut microbiota. Conclusion: The differences in gut microbiota between PCOS patients and controls vary across observational studies. However, MR analyses identified specific gut microbiota taxa that are causally related to PCOS. Future studies should investigate the gutmicrobiota that showed significant results in the MR analyses, as well as the underlying mechanisms of this causal relationship and its potential clinical significance. [ABSTRACT FROM AUTHOR]

The complex interaction between the gastrointestinal system and the central nervous system has become a captivating area of study, particularly about neurodegenerative diseases. This review critically examines the evolving understanding of the gut-brain axis and its significant implications for diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). The gut-brain axis represents a two-way communication system that involves neural, hormonal, and immunological pathways, which are mediated by the gut microbiota, microbial metabolites, and the enteric nervous system. Disruption of this axis has been implicated in the development and progression of neurodegenerative disorders. We delve into the role of gut dysbiosis in neuroinflammation, exploring how changes in the composition of the gut microbiota can trigger immune responses that affect neuronal function and survival. Additionally, we discuss the impact of microbial metabolites, such as short-chain fatty acids and neurotransmitters, on neuroprotective mechanisms, providing insight into the intricate communication between the gut and the brain. In the case of Alzheimer's disease, accumulating evidence suggests a connection between gut dysbiosis, amyloid-beta deposition, and neuroinflammation, opening up possibilities for microbiota-targeted interventions aimed at slowing down disease progression. Similarly, in Parkinson's disease, alterations in the composition of the gut microbiota have been linked to the aggregation of alpha-synuclein and motor dysfunction, indicating the potential therapeutic benefits of modulating the gut microbiota to alleviate symptoms and alter the course of the disease. [ABSTRACT FROM AUTHOR]

Background: There is no direct evidence of gut microbiota disturbance in children with gastroesophageal reflux disease (GERD). This study aimed to provide direct evidence and a comprehensive understanding of gut microbiota disturbance in children with GERD through combined metagenomic and metabolomic analysis. Methods: 30 children with GERD and 30 healthy controls (HCs) were continuously enrolled, and the demographic and clinical characteristics of the subjects were collected. First, 16S rRNA sequencing was used to evaluate differences in the gut microbiota between children with GERD and HC group, and 10 children with GERD and 10 children in the HC group were selected for metagenomic analysis. Nontargeted metabolomic analysis was performed using liquid chromatography/mass spectrometry (LC/MS), and metagenomic and metabolomic data were analyzed together. Results: There were significant differences in the gut microbiota diversity and composition between children with GERD and HCs. The dominant bacteria in children with GERD were Proteobacteria and Bacteroidota. At the species level, the top three core bacterial groups were Bacteroides stercoris, Bacteroides vulgatus and Alistipes putredinis. The main differential pathways were identified to be related to energy, amino acid, vitamin, carbohydrate and lipid metabolism. LC/MS detected 288 different metabolites in the positive and negative ion modes between children with GERD and HCs, which were mainly involved in arachidonic acid (AA), tyrosine, glutathione and caffeine metabolism. Conclusion: This study provides new evidence of the pathogenesis of GERD. There are significant differences in the gut microbiota, metabolites and metabolic pathways between HCs and children with GERD, and the differences in metabolites are related to specific changes in bacterial abundance. In the future, GERD may be treated by targeting specific bacteria related to AA metabolism. [ABSTRACT FROM AUTHOR]

Tuberculosis (TB), an airborne pulmonary disease caused by Mycobacterium tuberculosis (M. tb), poses an unprecedented health and economic burden to most of the developing countries. Treatment of TB requires prolonged use of a cocktail of antibiotics, which oftenmanifest several side effects, including stomach upset, nausea, and loss of appetite spurring on treatment non-compliance and the emergence of antibiotic resistant M. tb. The anti-TB treatment regimen causes imbalances in the composition of autochthonous microbiota associated with the human body, which also contributes to major side effects. The microbiota residing in the gastrointestinal tract play an important role in various physiological processes, including resistance against colonization by pathogens, boosting host immunity, and providing key metabolic functions. In TB patients, due to prolonged exposure to anti-tuberculosis drugs, the gut microbiota significantly loses its diversity and several keystone bacterial taxa. This loss may result in a significant reduction in the functional potency of the microbiota, which is a probable reason for poor treatment outcomes. In this review, we discuss the structural and functional changes of the gut microbiota during TB and its treatment. A major focus of the review is oriented to the gut microbial association with micronutrient profiles and immune cell dynamics during TB infection. Furthermore, we summarize the acquisition of anti-microbial resistance in M. tb along with the microbiome-based therapeutics to cure the infections. Understanding the relationship between these components and host susceptibility to TB disease is important to finding potential targets that may be used in TB prevention, progression, and cure. [ABSTRACT FROM AUTHOR]

The intestinal microbiome has a long-term symbiosis with the body, not only participating in the formation of the intestinal barrier, but also maintaining the body′s metabolism by producing vitamins and other products necessary for host physiology. Autophagy is a cellular catabolic process used to maintain homeostasis, and it functions at a fundamental level in all tissues. In this review, we will elaborate the changes of autophagy when regulating intestinal microbiome and the changes of intestinal microbiome when autophagy changes, so as to provide more research directions for the treatment of diseases. [ABSTRACT FROM AUTHOR]

Background: It is known that the gut microbiome of a healthy person affects the process of COVID-19 after getting infected with SARS-CoV-2 virus. It is also believed that colchicine can alleviate the severity of COVID-19. Objective: Current investigations aimed to evaluate the associations between the baseline gut microbiota composition of healthy and Familial Mediterranean fever (FMF) - carrier Armenian men populations, and the severity of the COVID-19 disease after their infection with the SARS-CoV-2. The study has a purpose of answering three core questions: i. Do the characteristics of gut microbiome of Armenians affect the course of COVID-19 severity? ii. How does the COVID-19 disease course on go for FMF patients who have been taking colchicine as a medication over the years after getting infected with SARS-CoV-2? iii. Is there an initial gut micribiota structure pattern for non-FMF and FMF patients in the cases when COVID-19 appears in mild form? Methods: The gut microbiota composition in non-FMF and FMF patients before the first infection (mild and moderate course of COVID-19) was considered. COVID-19 was diagnosed by SARS-CoV-2 nucleic acid RT-PCR in nasopharyngeal swab and/or sputum. Results: The number of patients with male FMF with mild COVID-19 was approximately two times higher than that of non-FMF male subjects with COVID-19. In addition, an association of COVID-19 disease severity with the baseline gut Prevotella, Clostridium hiranonis, Eubacterium biforme, Veillonellaceae, Coprococcus, and Blautia diversities in the non-FMF and FMF populations were revealed by us, which can be used as risk/prognostic factor for the severity of COVID-19. [ABSTRACT FROM AUTHOR]

The degrees to which the polysaccharide fucoidan (FUC) and its acid (AFUC) and oxidative degradation products (OFUC) are metabolized in the gut of BALB/c mice were investigated, and their effects on the gut metabolites were compared. High-performance liquid chromatography-tandem mass spectrometry measurement revealed the proportions of FUC, AFUC, and OFUC excreted in the mouse feces to be 48.85%, 40.78%, and 40.99%, respectively. Although the relative molecular mass of FUC did not have a significant effect on its excretion rate, there were large inter-individual differences. Furthermore, multiple linear regression analysis of the rates of FUC, AFUC, and OFUC metabolism in the gut revealed that AFUC was metabolized mainly by the Muribaculaceae, whereas FUC and OFUC were mainly utilized by the Lachnospiraceae, Muribaculaceae, and Bacteroidaceae. FUC,AFUC, and OFUC affected the metabolic activities of the gut microflora and jointly affected the D-glutamine and D-glutamate metabolic pathways in the host. OFUC andAFUC both significantly affected the pathway for biotin metabolism, indicating significant differences in gut microbiota interactions between FUC and its degradation products. This study reveals the mechanism by which FUC carries out its effects through the gut microbiota and provides data supporting further application of this polysaccharide and its degradation products in the food industry. [ABSTRACT FROM AUTHOR]

The effects of the established life-prolonging diet on human gut microbiota in Guangxi were investigated in this study.Atotal of 14 volunteers were screened and required to follow this diet for two weeks with high levels of compliance. Fecal samples were collected before and after the dietary intervention and analyzed using 16S rDNA high-throughput sequencing. The results show that the gut microbiota diversity of volunteers changed in multiple respects after the dietary intervention. At the phylum level, the relative abundance of TM7 significantly decreased (from 0.05%to 0.01%), and the relative abundance of Proteobacteria and the ratio of Firmicutes to Bacteroidetes also decreased. At the genus level, the relative abundance of Coprococcus increased significantly (from 1.04% to 1.39%), while the relative abundance of Escherichia (from 14.00%to 9.62%), Ruminococcus (from 5.67%to 2.48%), andMegamonas (from 4.06%to 0.04%) significantly decreased. Redundancy analysis indicated that changes in the gut microbiota were closely related to daily food consumption, with the average daily intake of vegetables being the most relevant (r²=0.89, p<0.01). The above results prove that the structure of human gut microbiota in Guangxi could be effectively regulated by the life-prolonging diet. Furthermore, the abundance of certain harmful bacteria in the intestinal tract was reduced, which has a positive effect on maintaining a healthy body. These results provide a reference for revealing an effective mechanism for regulating health and longevity through diet in terms of gutmicrobiota. [ABSTRACT FROM AUTHOR]

Obesity is a metabolic disease caused by the excessive fat accumulation and is a global health problem that affects more than one-third of the population. Probiotics are considered an effective alternate treatment for preventing obesity as FDA-approved anti-obesity drugs are associated with side effects, such as depression, diarrhea, and dyspepsia. Oral administration of Lacticaseibacillus paracasei AO356 (AO356) isolated from healthy female Koreans to high-fat diet-fed C57BL/6J male mice effectively ameliorated body weight gain, abnormal body composition, and obesity-induced hyperleptinemia and inflammation. This effect may be associated with the downregulation of adipogenesis transcription factor-and lipid metabolism related genes, such as Srebp1c, Pparγ, Fas, C/ebpα, and Fabp4 and upregulation of thermogenesis-related genes, such as Ucp1, Cpt1, Pgc1α, Cidea, and Prdm16 in epididymal and subcutaneous fat pads. In conclusion, our results show that AO356 prevents high-fat diet-induced obesity by regulating adipogenesis and thermogenesis.

Increasing evidence indicated that probiotics can be effective in improving behaviors similar to depression and anxiety disorders. However, the underlying mechanisms remain unclear, as is the effects of single vs. combined probiotics on depression and anxiety. This study aimed to determine whether combined probiotics could attenuate depressive-like and anxiety-like behavior induced by chronic unpredictable mild stress (CUMS) and its potential mechanisms. Rats underwent CUMS treatment and then administered Lactobacillus rhamnosus HN001 (HN001) or Bifidobacterium animalis subsp. lactis HN019 (HN019), alone or in combination. Levels of neurotransmitters, inflammatory factors, and the gut microbiota were measured. HN001 and (or) HN019 treatment improved depressive-like and anxiety-like behavior in rats, including increased moving distance and exploratory behavior (p < 0.05). In addition, altered gut microbiota structure induced by CUMS was amended by HN001 and/or HN019 (p < 0.05). HN001 and/or HN019 intervention also remarkably normalized levels of 5-HT, DA, NE, HVA, DOPAC, HIAA, TNF-a, IL-6, IL-18 and IL-1b in CUMS rats (p < 0.05). Furthermore, the effects of combined probiotics on decreasing inflammation and improved gut microbiota (Chao1 index and ACE index, p < 0.05) were superior to the single probiotics. Moreover, spearman analysis showed a certain correlation between the diFFerent microbiota, such as Firmicutes, Bacteroidetes, Verrucomicrobias, Proteobacterias and Actinobacterias, and inflammation and neurotransmitters. These findings suggested that CUMS induced depressive and anxiety-like behaviors can be alleviated by the combination of probiotics, which was possibly associated with the alterations in the gut microbiota composition and increased neurotransmitters and decreased inflammatory factors. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD) is a neurological disorder that affects normal brain development. The recent finding of the microbiota-gut-brain axis indicates the bidirectional connection between our gut and brain, demonstrating that gut microbiota can influence many neurological disorders such as autism. Most autistic patients suffer from gastrointestinal (GI) symptoms. Many studies have shown that early colonization, mode of delivery, and antibiotic usage significantly affect the gut microbiome and the onset of autism. Microbial fermentation of plant-based fiber can produce different types of short-chain fatty acid (SCFA) that may have a beneficial or detrimental effect on the gut and neurological development of autistic patients. Several comprehensive studies of the gut microbiome and microbiota-gut-brain axis help to understand the mechanism that leads to the onset of neurological disorders and find possible treatments for autism. This review integrates the findings of recent years on the gut microbiota and ASD association, mainly focusing on the characterization of specific microbiota that leads to ASD and addressing potential therapeutic interventions to restore a healthy balance of gut microbiome composition that can treat autism-associated symptoms. [ABSTRACT FROM AUTHOR]

This study administered the goji juice (20 mL/kg/d) fermented by Lactobacillus plantarum, Lactobacillus reuteri and Streptococcus thermophilus or unfermented juice for male mice for 30 days, then the effects on dextran sodium sulfate (DSS)-induced ulcerative colitis were investigated. The results shown that intaking fermented or unfermented goji juice decreased the levels of pro-inflammatory cytokines and total superoxide dismutase (T-SOD) in serum and colon, while increased the levels of anti-inflammatory cytokines, myeloperoxidase (MPO) and glutathione peroxidase (GSH). Additionally, intaking fermented or unfermented goji juices decreased intestinal permeability, and modulated gut microbiota at the phylums, family and genus level in ulcerative colitis mice. It is worth noting that the probiotics-fermented goji juice showed better anti-inflammatory effects than unfermented goji juice. These results demonstrated that probiotics-fermentation enhanced the anti-ulcerative colitis function of goji berry juice by regulating oxidative stress and inflammation markers and modulating gut microbiota.

The intestinal microbiota plays an important role in the occurrence and development of alcoholic liver disease (ALD). The aim of this study was to investigate whether the cornel iridoid glycoside (CIG) of Cornus officinalis Sieb. et Zucc. could protect against ALD through the gut-liver axis. The results showed that, compared to an alcohol treated group, CIG could inhibit the activities of AST, ALT and MDA, promote the activities of SOD, CAT and GSH, and reduce oxidative damage to the liver. CIG could significantly alter intestinal microbial diversity, reduce the presence of serum LPS and levels of TNF-α, IL-1β and IL-6 in the liver. In addition, CIG supplementation reduced the imbalance of intestinal microbiota caused by alcohol and improved intestinal barrier function. Therefore, CIG may have a beneficial effect in alcoholic liver disease by maintaining the stability of the intestinal microbiota. We propose CIG as a potential therapeutic and prophylactic compound in clinical treatment of ALD.

Researches on gut microbiota in autism have mostly focused on children, but the dynamic changes of gut microbiota from weaning to adulthood were still not clear because of the difficulty of diagnosing autism. In this study, autistic-like rats indued by valproate (VPA) were tracked from weaning (end of breastfeeding; four weeks old) to sexual maturation (food; eight weeks old). Autistic-like rats were found to show obvious developmental disorders. During weaning, autistic-like rats only exhibited obvious repetitive stereotyped behaviors, but the autistic-like behaviors were fully apparent upon sexual maturation. Significant differences were observed between the gut microbiota of autistic-like and healthy rats across both age groups. The correlation analysis results revealed that the correlation between behaviors and some microbiota, especially Helicobacter, did not vary with age or diet. The total amount of short-chain fatty acids (SCFAs) decreased, butyric acid metabolism decreased, and propionic acid metabolism increased in the feces of autistic-like rats. The correlation between autistic-like behaviors and the butyric acid and propionic acid levels did not vary with diet or age. Inositol phosphate metabolism, amino acid metabolism, and lipopolysaccharide biosynthesis were significantly associated with autistic-like behaviors. Our results showed that although the microbiota and SCFAs related to autism were affected by age and diet, some remained consistent irrespective of age and diet, and they could be considered two of the factors related to autistic-like behaviors development.

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Objective: Increasing evidence indicates that intestinal microbiota play a role in diverse metabolic processes via intestinal butyrate production. Human bariatric surgery data suggest that the gut-brain axis is also involved in this process, but the underlying mechanisms remain unknown. Methods: We compared the effect of fecal microbiota transfer (FMT) from post-Roux-en-Y gastric bypass (RYGB) donors vs oral butyrate supplementation on (123I-FP-CIT-determined) brain dopamine transporter (DAT) and serotonin transporter (SERT) binding as well as stable isotope-determined insulin sensitivity at baseline and after 4 weeks in 24 male and female treatment-naïve metabolic syndrome subjects. Plasma metabolites and fecal microbiota were also determined at these time points. Results: We observed an increase in brain DAT after donor FMT compared to oral butyrate that reduced this binding. However, no effect on body weight and insulin sensitivity was demonstrated after post-RYGB donor feces transfer in humans with metabolic syndrome. Increases in fecal levels of Bacteroides uniformis were significantly associated with an increase in DAT, whereas increases in Prevotella spp. showed an inverse association. Changes in the plasma metabolites glycine, betaine, methionine, and lysine (associated with the S-adenosylmethionine cycle) were also associated with altered striatal DAT expression. Conclusions: Although more and larger studies are needed, our data suggest a potential gut microbiota-driven modulation of brain dopamine and serotonin transporters in human subjects with obese metabolic syndrome. These data also suggest the presence of a gut-brain axis in humans that can be modulated. NTR registration: 4488.

Acne vulgaris has been postulated to have a gastrointestinal mechanism; however, little is known about gut microbiota dysfunction in this condition. The aim of this cross-sectional study was to investigate whether the gut microbiota is altered in acne. Faecal bacterial diversity was analysed in 43 patients with acne and 43 controls, using hypervariable tag sequencing of the V3–V4 region of the 16S rDNA gene. Distinct differences were found in microbial diversity between patients with acne and controls (Shannon diversity index (p = 0.009) and Simpson diversity index (p = 0.01)). At the phylum level, the abundance of Firmicutes was lower in the patient group, but that of Bacteroidiain was higher. The most significantly depleted taxa in acne were Clostridia, Clostridiales, Lachnospiraceae and Ruminococcaceae genera, which are potentially beneficial. In conclusion, patients with acne vulgaris have gut microbial dysbiosis; further study is needed to understand its role in the pathogenesis of acne.

The freshwater pulmonate snail Planorbella trivolvis is a common species in various bodies of water but is not native to China. Planorbella trivolvis usually live on diets with high fiber content, such as water grasses, algae and fallen leaves. These snails can attach to the wall of a water tank or to water grass and can be transported overseas to China through the ornamental fish trade. There are few studies investigating the intestinal microbiota of freshwater snails. In this study, using culture-independent molecular analysis, we assessed for the first time the complexity of bacterial communities in the intestines of reared snails. The intestinal microbiota in the snails fed different diets, that is, herbivorous feed (HV) with high cellulose and non-herbivorous feed (NHV) with low cellulose, were analyzed by Illumina sequencing. The results showed that the NHV-based diet significantly increased the body mass, shell diameter and specific growth rate of the snails after 60 days of rearing (P < 0.05). Histological experiments showed that the fat droplets in the epithelium columnar cells of the intestines of the NHV snails increased, and the cilia on these cells fell off. The sequencing results identified 486 and 195 OTUs in HV and NHV, respectively. Lots of bacteria were not reported previously in snails. The intestinal microbiota diversity index (Shannon, Simpson, Ace and Chao) in the NHV snails was significantly lower than that in the HV snails. The gut microbiota in the HV snails were predominantly Proteobacteria (52.97%) and Bacteroidetes (28.75%), while the gut microbiota in NHV snails were predominantly Proteobacteria (95.23%). At the genus level, Cloacibacterium (24.60%), Pseudomonas (4.47%), OM6ON (6.12%), and Rhodobacter (5.79%) were observed to be abundant in HV snails. However, Aeromonas (85.4%) was determined to be predominant in NHV snails. Functional prediction of the gut microbiome in snails by PICRUSt demonstrated a significant difference between the two groups, and the HV snails exhibited higher lignocellulose enzyme activity than did the NHV snails. This study represents a first step in characterizing the gut microbiota of the freshwater snail. Most of these microbes can process plant biomass and digest cellulose and lignocellulose, and the enzymes of these bacteria may have potential biotechnological applications in a variety of industrial processes. [ABSTRACT FROM AUTHOR]

Gut microbiota has been proved to be an indispensable link between nutrient excess and metabolic syndrome, and chitin oligosaccharide (NACOS) has displayed therapeutic effects on multiple diseases such as cancer and gastritis. In this study, we aim to confirm whether NACOS can ameliorate high-fat diet (HFD)-induced metabolic syndrome by rebuilding the structure of the gut microbiota community. Male C57BL/6J mice fed with HFD were treated with NACOS (1 mg/mL) in drinking water for five months. The results indicate that NACOS improved glucose metabolic disorder in HFD-fed mice and suppressed mRNA expression of the protein regulators related to lipogenesis, gluconeogenesis, adipocyte differentiation, and inflammation in adipose tissues. Additionally, NACOS inhibited the destruction of the gut barrier in HFD-treated mice. Furthermore, 16S ribosome RNA sequencing of fecal samples demonstrates that NACOS promoted the growth of beneficial intestinal bacteria remarkably and decreased the abundance of inflammogenic taxa. In summary, NACOS partly rebuilt the microbial community and improved the metabolic syndrome of HFD-fed mice. These data confirm the preventive effects of NACOS on nutrient excess-related metabolic diseases. [ABSTRACT FROM AUTHOR]

[Display omitted] • Lacticaseibacillus paracasei AO356 decreased high-fat diet-induced body weight gain, and fat mass. • Lacticaseibacillus paracasei AO356 decrease adipocyte size and increase skeletal muscle fiber size in C57BL/6J male mice. • Lacticaseibacillus paracasei AO356 downregulated the expression of adipogenesis transcription factors in epididymal and subcutaneous fat pads. • Lacticaseibacillus paracasei AO356 upregulated the expression of thermogenesis-related genes in epididymal and subcutaneous fat pads. Obesity is a metabolic disease caused by the excessive fat accumulation and is a global health problem that affects more than one-third of the population. Probiotics are considered an effective alternate treatment for preventing obesity as FDA-approved anti-obesity drugs are associated with side effects, such as depression, diarrhea, and dyspepsia. Oral administration of Lacticaseibacillus paracasei AO356 (AO356) isolated from healthy female Koreans to high-fat diet-fed C57BL/6J male mice effectively ameliorated body weight gain, abnormal body composition, and obesity-induced hyperleptinemia and inflammation. This effect may be associated with the downregulation of adipogenesis transcription factor-and lipid metabolism related genes, such as Srebp1c , Pparγ , Fas , C/ebpα , and Fabp4 and upregulation of thermogenesis-related genes, such as Ucp1 , Cpt1 , Pgc1α , Cidea , and Prdm16 in epididymal and subcutaneous fat pads. In conclusion, our results show that AO356 prevents high-fat diet-induced obesity by regulating adipogenesis and thermogenesis. [ABSTRACT FROM AUTHOR]

Objective To evaluate the distribution of intestinal flora in patients with cirrhosis compared with healthy people and investigate the relationship between the distribution of intestinal flora and Child- Pugh classification of liver function,and to analyze the effect of probiotic treatment on the improvement of intestinal flora and liver biochemical indices in patients with cirrhosis. Methods Twenty- six patients with compensated cirrhosis( without ascites) and 22 with decompensated cirrhosis( with ascites) who were admitted to our hospital from February 2014 to July 2014,as well as 21 healthy adult subjects,were randomly selected. Patients with cirrhosis were given probiotic( Bei Feida) treatment in addition to conventional therapy for 14 days. All patients signed informed consent forms. The distribution of intestinal flora,blood ammonia,serum alanine aminotransferase,serum albumin,and serum bilirubin levels were determined. Comparison of continuous data between the two and multiple groups was made by t test and analysis of variance,respectively,and comparison of categorical data was made by non-parametric test. Results All patients with cirrhosis had varying degrees of intestinal dysbacteriosis,predominantly due to significantly increased enterococci and enteric bacilli( P < 0. 01) and significantly reduced bifidobacteria( P < 0. 01). Dysbacteriosis was associated with liver function. Patients with Child- Pugh C cirrhosis had significantly more severe dysbacteriosis than patients with Child- Pugh A cirrhosis( P <0. 01). Probiotic treatment significantly improved liver biochemical indices,reduced blood ammonia,and increased intestinal bifidobacteria( P <0. 01). Probiotic treatment improved the Child- Pugh classification in patients with cirrhosis and had a more significant effect on cirrhotic patients with ascites( P < 0. 01). Conclusion Patients with cirrhosis have varying degrees of intestinal dysbacteriosis. Probiotic treatment can effectively relieve dysbacteriosis,improve biochemical indices,and reduce blood ammonia in patients with cirrhosis. [ABSTRACT FROM AUTHOR]

Recent studies reveal a potential contribution of intestinal microbes in the expression of certain human cardio-metabolic diseases. The mechanisms through which intestinal microbiota and/or their metabolic products alter systemic homoeostasis and cardio-metabolic disease risks are just beginning to be dissected. Intervention studies in humans aiming to either selectively alter the composition of the intestinal microbiota or to pharmacologically manipulate the microbiota to influence production of their metabolites are crucial next steps. The intestinal microbiome represents a new potential therapeutic target for the treatment of cardio-metabolic diseases. [ABSTRACT FROM PUBLISHER]

There has been growing interest in the use of fecal microbiota for the treatment of patients with chronic gastrointestinal infections and inflammatory bowel diseases. Lately, there has also been interest in its therapeutic potential for cardiometabolic, autoimmune, and other extraintestinal conditions that were not previously considered to be associated with the intestinal microbiota. Although it is not clear if changes in the microbiota cause these conditions, we review the most current and best methods for performing fecal microbiota transplantation and summarize clinical observations that have implicated the intestinal microbiota in various diseases. We also discuss case reports of fecal microbiota transplantations for different disorders, including Clostridium difficile infection, irritable bowel syndrome, inflammatory bowel diseases, insulin resistance, multiple sclerosis, and idiopathic thrombocytopenic purpura. There has been increasing focus on the interaction between the intestinal microbiome, obesity, and cardiometabolic diseases, and we explore these relationships and the potential roles of different microbial strains. We might someday be able to mine for intestinal bacterial strains that can be used in the diagnosis or treatment of these diseases. [Copyright &y& Elsevier]

[Display omitted] • The fermented and unfermented goji berry juices attenuated dextran sodium sulfate induced colitis. • The probiotics-fermented goji berry juice treatment (FGJ, 20 mL/kg/d) prevented histological damage. • FGJ enhanced intestinal integrity and modulated inflammatory cytokines in serum and colon. • The key gut bacteria at the phylums, family and genus level were regulated by FGJ. This study administered the goji juice (20 mL/kg/d) fermented by Lactobacillus plantarum , Lactobacillus reuteri and Streptococcus thermophilus or unfermented juice for male mice for 30 days, then the effects on dextran sodium sulfate (DSS)-induced ulcerative colitis were investigated. The results shown that intaking fermented or unfermented goji juice decreased the levels of pro-inflammatory cytokines and total superoxide dismutase (T-SOD) in serum and colon, while increased the levels of anti-inflammatory cytokines, myeloperoxidase (MPO) and glutathione peroxidase (GSH). Additionally, intaking fermented or unfermented goji juices decreased intestinal permeability, and modulated gut microbiota at the phylums, family and genus level in ulcerative colitis mice. It is worth noting that the probiotics-fermented goji juice showed better anti-inflammatory effects than unfermented goji juice. These results demonstrated that probiotics-fermentation enhanced the anti-ulcerative colitis function of goji berry juice by regulating oxidative stress and inflammation markers and modulating gut microbiota. [ABSTRACT FROM AUTHOR]

[Display omitted] • Protective effect of iridoid glycoside extracted from Cornus officinalis on liver. • Cornel iridoid glycoside regulate oxidative stress and inflammation in liver. • Cornel iridoid glycoside maintain intestinal health. • Potential mechanism of cornel iridoid glycoside anti-alcoholic liver injury. The intestinal microbiota plays an important role in the occurrence and development of alcoholic liver disease (ALD). The aim of this study was to investigate whether the cornel iridoid glycoside (CIG) of Cornus officinalis Sieb. et Zucc. could protect against ALD through the gut-liver axis. The results showed that, compared to an alcohol treated group, CIG could inhibit the activities of AST, ALT and MDA, promote the activities of SOD, CAT and GSH, and reduce oxidative damage to the liver. CIG could significantly alter intestinal microbial diversity, reduce the presence of serum LPS and levels of TNF-α, IL-1β and IL-6 in the liver. In addition, CIG supplementation reduced the imbalance of intestinal microbiota caused by alcohol and improved intestinal barrier function. Therefore, CIG may have a beneficial effect in alcoholic liver disease by maintaining the stability of the intestinal microbiota. We propose CIG as a potential therapeutic and prophylactic compound in clinical treatment of ALD. [ABSTRACT FROM AUTHOR]

Increasing evidence indicates that intestinal microbiota play a role in diverse metabolic processes via intestinal butyrate production. Human bariatric surgery data suggest that the gut-brain axis is also involved in this process, but the underlying mechanisms remain unknown. We compared the effect of fecal microbiota transfer (FMT) from post-Roux-en-Y gastric bypass (RYGB) donors vs oral butyrate supplementation on (123I-FP-CIT-determined) brain dopamine transporter (DAT) and serotonin transporter (SERT) binding as well as stable isotope-determined insulin sensitivity at baseline and after 4 weeks in 24 male and female treatment-naïve metabolic syndrome subjects. Plasma metabolites and fecal microbiota were also determined at these time points. We observed an increase in brain DAT after donor FMT compared to oral butyrate that reduced this binding. However, no effect on body weight and insulin sensitivity was demonstrated after post-RYGB donor feces transfer in humans with metabolic syndrome. Increases in fecal levels of Bacteroides uniformis were significantly associated with an increase in DAT, whereas increases in Prevotella spp. showed an inverse association. Changes in the plasma metabolites glycine, betaine, methionine, and lysine (associated with the S -adenosylmethionine cycle) were also associated with altered striatal DAT expression. Although more and larger studies are needed, our data suggest a potential gut microbiota-driven modulation of brain dopamine and serotonin transporters in human subjects with obese metabolic syndrome. These data also suggest the presence of a gut-brain axis in humans that can be modulated. 4488. What is already known about this subject? • Gut microbiota are involved in human health and metabolic disease. • Changes in gut microbiota are associated with brain disease. • Animal studies have suggested that fecal transplantation can alter brain (dopamine and serotonin) metabolism. What are the new findings? • Donor fecal microbiota transplantation affects (123I-FP-CIT-determined) cerebral serotonin transporters (SERT) and dopamine transporters (DAT) in obese humans with metabolic syndrome. • These differential changes are accompanied by alterations in plasma metabolites and fecal microbiota composition. • New correlations between changes in microbiota strains and plasma metabolites in relation to the gut-brain axis in human obesity are observed. How might it impact on clinical practice in the foreseeable future? • This study helps to quantify the magnitude of gut microbiota-driven effects on human serotonin and dopamine in obese humans. • This study provides a rationale for future sample size calculations for FMT trials in manipulating the gut-brain axis through gut microbiota interventions. • This study provides a rationale for future sample size calculations for FMT trials in manipulating the gut-brain axis through gut microbiota interventions. [ABSTRACT FROM AUTHOR]